scholarly journals Pituitary Hyperplasia Secondary to Primary Hypothyroidism Mimicking a Macroadenoma With Optical Chiasm Compression

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A599-A600
Author(s):  
Mariana Tazima Fujiwara ◽  
Karla Borges Daniel ◽  
Marília Bortolotto Felippe Trentin ◽  
Murilo Oliveira Cerci ◽  
Heraldo Mendes Garmes
Keyword(s):  
Case Report ◽  
Thyroid Function ◽  
Sella Turcica ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Psychomotor Development ◽  
Normal Range ◽  
Pituitary Hyperplasia ◽  
Pituitary Lesion

Abstract Background: A long term untreated primary hypothyroidism can stimulate thyrotropes proliferation, leading to pituitary hyperplasia. This condition is known as pituitary hyperplasia secondary to primary hypothyroidism (PHPH). It is a rare condition that mimics pituitary adenoma and can achieve large proportions with optic chiasm compression. A misdiagnosis may be catastrophic, and a pituitary resection wrongly performed. Clinical Case: A 25-year-old woman with a medical history of delayed neuro psychomotor development and epilepsy due to congenital CNS malformation had a Brain MRI performed for epilepsy follow-up three years earlier. At that time, neuroimaging had shown a pituitary enlargement, and laboratory data were diagnostic of severe primary hypothyroidism with TSH of 290.6 uUI/mL (normal range 0.4 to 4.5 uUI/mL) and T4L <0.23 ng/dL (normal range: 0.9 to 1.8 ng/dL). She then had received a 75 mcg levothyroxine prescription. However, the patient missed medical follow-up and returned three years later, when sella turcica MRI showed a 0.9x1.0x1,4 cm pituitary lesion, consistent with a macroadenoma with suprasellar extent near the optic chiasm. Because of the cognitive impairment, the patient was not able to complete the visual field test. Neurology service referred the patient to endocrinology evaluation for surgical treatment. Hypothyroidism was still uncontrolled with TSH 157.1 uUI/mL and T4L 0.28 ng/dL. We had adjusted the levothyroxine dose to 125 mcg and advised adherence. Subsequent thyroid function tests had shown TSH 6.91 uUI/mL and T4L 1.15 ng/dL. After thyroid function stabilization, the patient performed a new sella turcica MRI, which had not evidenced pituitary lesion. Pituitary hyperplasia secondary to primary hypothyroidism was her final diagnosis. Conclusion: This case report illustrates the importance of the correct diagnosis and treatment of PHPH. Levothyroxine replacement, with TSH normalization, reverses the gland hyperplasia within 2 to 4 months. References: 1. Cao J, Lei T, Chen F, Zhang C, Ma C, Huang H. Primary hypothyroidism in a child leads to pituitary hyperplasia: A case report and literature review. Medicine (Baltimore). 2018 Oct;97(42):e12703.2. Shivaprasad KS, Siddardha K. Pituitary Hyperplasia from Primary Hypothyroidism. N Engl J Med. 2019 Feb 21;380(8):e9.

scholarly journals SUN-290 Pituitary Hyperplasia Due to Uncontrolled Primary Hypothyroidism: Case Series and Literature Review

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Juan Pablo Godoy Alonso ◽  
Germán González de la Cruz ◽  
Marlon Vladimir Vázquez-Aguirre ◽  
Andrea Rocha Haro ◽  
Karla Krystel Ordaz Candelario ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Feedback Inhibition ◽  
Case Series ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Autoimmune Hypothyroidism ◽  
Hormonal Replacement ◽  
Pituitary Hyperplasia ◽  
History Of

Abstract Background: Pituitary hyperplasia secondary to primary hypothyroidism results from the loss of thyroxine feedback inhibition and the subsequent overproduction of TSH. Case 1: A 18-year-old female presented with a chronic history of spontaneous galactorrhea, headache and malaise. Autoimmune primary hypothyroidism was diagnosed, with elevated TSH of 490 mIU/L (0.3-5) and low fT4 of 0.33 ng/dL (0.63-1.34). Pituitary MRI showed an enlarged pituitary with compression of the optic chiasm. Hormonal replacement with levothyroxine 75 mcg qd was started. Five months later she was asymptomatic, and normal TSH (1.64 mIU/L) and fT4 (0.9 ng/dL) levels. A new MRI revealed normal size of pituitary gland, with no compression of the optic chiasm and an intact infundibulum. Case 2: A 24-year-old female with type 1 diabetes and autoimmune primary hypothyroidism, presented with a five-year history of galactorrhea and oligomenorrhea. She was treated with insulin glargine 20U qd, and levothyroxine 200 mcg/day. However, patient’s adherence was bad. She consulted a primary health physician who suspected a prolactinoma after high prolactin levels (77.65, normal 2.64-13.13 ng/mL). Cabergoline was started without any clinical improvement. She then was referred to our service for follow-up. TSH results showed 500 mIU/L, with low fT4 (0.08 ng/dL). Prolactin levels was normal. Pituitary MRI revealed diffuse enlargement of the gland, with compression of infundibulum and optic chiasm. Treatment was modified to levothyroxine/liothyronine 100/20mcg 1 ½ tablet qd. After 7 months, we confirmed normal TSH (0.76 mIU/L) and fT4 (1.23 ng/dL), and the patient was asymptomatic. After 17 months, new MRI showed normal pituitary gland without any compression. Case 3: A 23-year-old female with a history of Addison′s disease and hypothyroidism diagnosed at age 17 presented with a 6-month history of somnolence, fatigue, headache and amenorrhea. She was previously treated with hydrocortisone 25mg/day, fludrocortisone 0.1mg/day, and levothyroxine 200mcg/day. Patient’s adherence was bad, and multiple hospitalizations because of adrenal crises were reported. Her initial hormonal evaluation revealed high TSH of 460 mIU/L and low fT4 of 0.25 ng/dL, mild hyperprolactinemia (32.16 ng/mL), and very high ACTH levels (2,700 pg/mL, normal 10-100). Pituitary MRI revealed an enlarged pituitary with mild compression of the optic chiasm. Hormonal replacement was modified to fasting levothyroxine alternating 200mcg and 300mcg qd. Her last follow-up showed normal TSH (0.53 mIU/L) and fT4 (1.18 ng/dL) levels. New MRI showed normal pituitary size Conclusion: We presented three young women, with autoimmune hypothyroidism, who developed pituitary hyperplasia and responded to proper hormonal replacement normalizing pituitary size. Reference: Endocrinol Diabetes Metab Case Rep. 2015; 2015: 150056.

scholarly journals SAT-467 A Case of Pituitary Hyperplasia Secondary to Uncontrolled Primary Hypothyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hebah Alhumaidi ◽  
Sarika Rao ◽  
Dhruv Kansal
Keyword(s):  
Ethinyl Estradiol ◽  
Field Testing ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Pituitary Macroadenoma ◽  
Pituitary Hyperplasia ◽  
Morning Cortisol ◽  
Free Cortisol ◽  
Slight Elevation

Abstract 17 year old female presented for evaluation of galactorrhea of 3 months duration. Patient was diagnosed with papillary thyroid cancer and underwent total thyroidectomy in 2011. She was prescribed Synthroid 175 mcg but was not compliant with taking her medicine. In April 2019 she developed bilateral galactorrhea for which she was evaluated at an outside facility and was found to have a prolactin 143.7ng/mL (n 7.2-63) and TSH 996 mIU/L (n 0.5 -4.0). Pituitary MRI revealed pituitary macroadenoma measuring 1.5 x 1.4 x 1.2 cm with slight elevation of the optic chiasm and infundibulum. She was advised to restart Synthroid and was referred for the neurosurgery team at our facility for surgical resection of pituitary macroadenoma. Over the same period of time, she gained 25 lbs, developed headaches, excessive fatigue, constipation, hair loss, lower extremity swelling, and puffiness of her face. Her menstrual cycles were regular but this was only after she was placed on norelgestromin/ ethinyl estradiol transdermal patch. She denied visual changes. By the time she was seen at our clinic in June 2019, she was taking Synthroid daily for 1 month. TSH decreased to 1.0 mIU/L and prolactin improved to 68 ng/mL. IGF-1 was low at 98 ng/mL (n 149-509). ACTH, morning cortisol, and 24 hour urine free cortisol were within reference range. Visual field testing showed no visual defects. We advised patient to continue taking Synthroid and to follow up in 1 month. On the follow up visit in July 2019, TSH was 0.2 mIU/L, prolactin was 52 ng/mL and IGF-1 was 105 ng/mL. Pituitary MRI showed pituitary hyperplasia that has decreased compared to previous MRI, now measuring around 1 cm at the largest dimension without contact with the optic chiasm and the Infundibulum was at midline. Galactorrhea and headaches resolved and fatigue significantly improved.

scholarly journals MON-058 Precocious Puberty and Hypothyroidism in a Pediatric Case

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jessica L Sea ◽  
Michael J Head ◽  
Harvey Kenn Chiu
Keyword(s):  
Precocious Puberty ◽  
Mass Effect ◽  
Optic Chiasm ◽  
Large Mass ◽  
Primary Hypothyroidism ◽  
Serum Prolactin ◽  
Free T4 ◽  
Pituitary Hyperplasia ◽  
Suprasellar Extension

Abstract Background: Hypothyroidism with secondary sellar/suprasellar mass is rarely associated with precocious puberty. Here we describe a rare case of pediatric hyperprolactinemia and precocious puberty secondary to hypothyroidism, marked TSH elevation, and pituitary hyperplasia. Clinical Case: A 9-year-old female, with onset of thelarche and menses occurring at age 7 and 8 respectively, presented with primary hypothyroidism (Free T4 <0.11; n=4.9-11.4mcg/mL), elevated TSH (1620.0mU/mL; n=0.3-4.7mU/mL), hyperprolactinemia (108.6ng/mL; n=3.0-23.1ng/mL), and elevated serum estradiol (37.6pg/mL; n=10pg/mL). The patient had coarse scaly skin, diminished energy, and poor growth lasting 1 year. There were no associated gastrointestinal issues, temperature intolerance, nor visual impairments noted during this time. Magnetic resonance imaging revealed a large mass (1.48cm) with suprasellar extension and a mass effect on the optic chiasm. The patient was then started on Levothyroxine and Cabergoline, to reduce serum prolactin levels. However, upon follow-up two months later, the patient had hypoprolactinemia (2.0ng/mL; n=3.0-23.1ng/mL). The patient was referred to neurosurgery for resection of the sellar mass. Endocrinology was also consulted, at which point Cabergoline was discontinued and Levothyroxine was gradually increased. Follow up 4 months later showed prolactin levels had normalized to 11.4ng/mL (3.0-23.1ng/mL). Serum LH and FSH were within normal ranges (1.2mIU/mL and 4.2mIU/mL, respectively). TSH, though still elevated (47.35mU/mL; n=0.3-4.7mU/mL), was significantly reduced compared to the prior measurement (1620mU/mL). Serum levels of Free T4 increased to 1.06mcg/mL (n=4.9-11.4mcg/mL). Levothyroxine was titrated up and a repeated pituitary MRI demonstrated a significant decrease in the size of the mass with resolution of the suprasellar extension and mass effect on the optic chiasm. Further, the patient’s menses ceased and thelarche resolved upon correction of T4 and regression of the pituitary mass. Conclusions: While rare, primary hypothyroidism and TSH-driven pituitary hyperplasia can result in a large mass effect with suprasellar extension, causing secondary hyperprolactinemia by a mass effect and central precocious puberty. This case highlights the benefits for evaluating underlying hypothyroidism as a cause for hyperprolactinemia and sellar/suprasellar mass.

scholarly journals Case Report: De Quervain’s Thyroiditis as a Long-Term Sequelae Complication to SARS-CoV-2 Infection

2021 ◽  
pp. 64-70
Author(s):  
Mark Kong ◽  
Sarah La Porte
Keyword(s):  
Case Report ◽  
Thyroid Function ◽  
Elevated Serum ◽  
Subacute Thyroiditis ◽  
Thyroid Function Tests ◽  
Thyroid Function Testing ◽  
Neck Lump ◽  
Function Testing

A 44-year-old man presented with an enlarged painful lower anterior neck lump with elevated serum concentrations of free thyroxine (T4) and tri-iodothyronine (T3), alongside the presence of antithyroid peroxidase antibodies. Prior to presentation, the patient was demonstrating recovery from a SARS-CoV-2 infection that required sedation, intubation, and invasive ventilation in the intensive care unit (ICU) for 11 days. Ultrasound examination of the thyroid demonstrated features of De Quervain’s (subacute) thyroiditis. This corresponded to the clinical picture, and continuous thyroid function tests were arranged. Emerging evidence throughout the SARS-CoV-2 pandemic describes the long-term sequelae of the infection, including developing atypical effects on the thyroid gland. This case report emphasises the association of painful subacute thyroiditis with post-viral infection and its manifestation during recovery from severe SARS-CoV-2, suggesting that follow-up thyroid function testing should be considered in patients discharged from the ICU who develop neck discomfort.

scholarly journals Low Growth Hormone Levels in Short-Stature Children with Pituitary Hyperplasia Secondary to Primary Hypothyroidism

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Minghua Liu ◽  
Yanyan Hu ◽  
Guimei Li ◽  
Wenwen Hu
Keyword(s):  
Thyroid Hormones ◽  
Short Stature ◽  
Primary Hypothyroidism ◽  
Thyroid Antibodies ◽  
Gh Secretion ◽  
Pituitary Hyperplasia ◽  
Stimulation Tests ◽  
The Mean ◽  
Tsh Levels

Objective. The follow-up of GH levels in short-stature children with pituitary hyperplasia secondary to primary hypothyroidism (PPH) is reported in a few cases. We aimed to observe changes in GH secretion in short-stature children with PPH. Methods. A total of 11 short-stature children with PPH accompanied by low GH levels were included. They received levothyroxine therapy after diagnosis. Their thyroid hormones, IGF-1, PRL, and pituitary height were measured at baseline and 3 months after therapy. GH stimulation tests were performed at baseline and after regression of thyroid hormones and pituitary. Results. At baseline, they had decreased GH peak and FT3 and FT4 levels and elevated TSH levels. Decreased IGF-1 levels were found in seven children. Elevated PRL levels and positive thyroid antibodies were found in 10 children. The mean pituitary height was 14.3±3.8 mm. After 3 months, FT3, FT4, and IGF-1 levels were significantly increased (all p<0.01), and values of TSH, PRL, and pituitary height were significantly decreased (all p<0.001). After 6 months, pituitary hyperplasia completely regressed. GH levels returned to normal in nine children and were still low in two children. Conclusion. GH secretion can be resolved in most short-stature children with PPH.

scholarly journals Associations between thyroid function and mortality: the influence of age

2014 ◽  
Vol 171 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Annenienke C van de Ven ◽  
Romana T Netea-Maier ◽  
Femmie de Vegt ◽  
H Alec Ross ◽  
Fred C G J Sweep ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Age Groups ◽  
Population Based ◽  
Normal Range ◽  
Population Based Study ◽  
Middle Range ◽  
The Relationship ◽  
Subclinical Thyrotoxicosis ◽  
Tsh Levels

ObjectiveThe aim of this study was to investigate the influence of age on the association between thyroid function and mortality.DesignThe Nijmegen Biomedical Study is a population-based study, comprising 5816 randomly selected adults of all age groups without previously known thyroid disease.MethodsTSH, free thyroxine (FT4) and peroxidase antibodies were measured in 2002–2003. The number of deaths were established in 2012 (median follow-up time 9.4 years).ResultsSubclinical thyrotoxicosis was associated with mortality in subjects aged <65 years (hazard ratio (HR) 2.5, 95% CI 1.1–5.7), but not in subjects aged >65 years. As for thyroid function within the normal range: in the 493 participants aged 80 years or older, an FT4 level in the high-normal range (18.5–22 pmol/l) was associated with a higher mortality in comparison with FT4 levels in the middle range (11.5–15.0 pmol/l): HR 1.7 (95% CI 1.0–2.9). In these elderly, TSH levels within the high-normal range (3.0–4.0 mIU/l) were also associated with a higher mortality in comparison with TSH levels within the middle range (1.0–2.0 mIU/l): HR 1.8 (95% CI 1.0–3.1).ConclusionsThe relationship between thyroid function and mortality differs according to age. This finding might (partially) explain the discrepant results of previous studies examining the relationship between thyroid function and mortality in different age groups.

scholarly journals SUN-277 Pituitary Hyperplasia Due to Severe Primary Hypothyroidism: An Uncommon Manifestation of a Common Disease

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Abhilasha Singh ◽  
Massiell German ◽  
Anu Sharma
Keyword(s):  
Visual Field ◽  
Negative Feedback ◽  
Brain Mri ◽  
Subsequent Development ◽  
Optic Chiasm ◽  
Primary Hypothyroidism ◽  
Serum Prolactin ◽  
Visual Field Defects ◽  
Common Disease ◽  
Pituitary Hyperplasia

Abstract Background Pituitary hyperplasia (PH) is a non-neoplastic increase in one or more cell subtype of the adenohypophysis. It is physiologically seen in pregnancy from resultant lactotroph hyperplasia and pathologically in organ dysfunctions that lead to loss of negative feedback on hypothalamus like primary hypothyroidism and primary adrenal insufficiency. Although primary hypothyroidism is common, PH is an under-recognized consequence of long-standing hypothyroidism. Case Description A 26-year-old female with class 3 obesity, type 2 diabetes mellitus, and primary hypothyroidism on replacement presented for evaluation of secondary amenorrhea. Two months prior to presentation, she underwent a brain MRI for new-onset headache which revealed diffusely enhancing homogenous pituitary tissue measuring 2.3 cm with upward lifting of the optic chiasm. Serum prolactin was elevated at 86.2 ng/ml (2.8-26 ng/ml). This was presumed to be secondary to a prolactinoma and cabergoline was started by the referring provider. Subsequent workup revealed elevated thyroid-stimulating hormone (TSH) at 494.11 mU/L (0.30- 4.00 mU/L) and a low free thyroxine (FT4) of 0.2 ng/dl (0.8-1.7 ng/dl). Other pituitary hormones were within normal limits. The visual field examination was normal. It was noted she had a persistently elevated TSH over the past five years. On further questioning, the patient ran out of levothyroxine replacement 6 months ago and had been generally non-adherent to therapy for years due to nausea. Improved medication adherence resulted in the normalization of prolactin and reduction in TSH level. Repeat MRI 2 months later revealed a reduction in her pituitary hyperplasia to 2.1 cm. Discussion In severe primary hypothyroidism, there is loss of negative feedback to the hypothalamus due to low circulating FT4 and triiodothyronine (T3) concentrations. As a result, there is stimulation of thyrotropin-releasing hormone (TRH) which promotes thyrotroph hyperplasia. A strong correlation exists between TSH concentration and the degree of pituitary hyperplasia. The typical MRI finding is a diffusely enhancing homogenous pituitary mass. Despite optic chiasm contact, physiologic pituitary hyperplasia rarely causes visual field defects. High concentrations of TRH stimulates prolactin release with resultant mild hyperprolactinemia. Although PH is reversible with therapy, rare cases with subsequent development of panhypopituitarism while on therapy have been reported in the setting of longstanding hypothyroidism. Very rarely, chronically untreated primary hypothyroidism can stimulate the growth of a thyrotroph adenoma. Long-term biochemical and radiological monitoring is therefore recommended until resolution. This case highlights the physiologic responses manifested in severe primary hypothyroidism and the fact that these changes improve with adequate replacement.

Benign Neonatal Sleep Myoclonus: Case Report and Follow-up of Four Members of an Affected Family

2003 ◽  
Vol 34 (1) ◽  
pp. 15-17 ◽  
Author(s):  
M. Luigia Vaccario ◽  
Maria A. Valenti ◽  
Anna Carullo ◽  
Rossella Di Bartolomeo ◽  
Salvatore Mazza
Keyword(s):  
Case Report ◽  
Neurological Examination ◽  
Rem Sleep ◽  
Cognitive Functions ◽  
Psychomotor Development ◽  
Spontaneous Disappearance

Benign neonatal sleep myoclonus (BNSM), characterized by myoclonic jerks of the extremities only in non-REM sleep, occurs in the first months of life with spontaneous disappearance within 3–4 months. We examined five siblings with typical BNSM, at the 3–10 years follow-up neurological examination. Psychomotor development, cognitive functions and EEG were completely normal. These cases confirm that BNSM is a self limited and nonepileptic disorder.

scholarly journals A corticotroph pituitary adenoma as the initial presentation of familial glucocorticoid deficiency

2009 ◽  
Vol 161 (1) ◽  
pp. 195-199 ◽  
Author(s):  
Isabelle Benoit ◽  
Delphine Drui ◽  
Lucy Chaillous ◽  
Benoît Dupas ◽  
Jean-François Mosnier ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Tumour Size ◽  
Optic Chiasm ◽  
Initial Presentation ◽  
Pituitary Hyperplasia ◽  
Magnetic Resonance Imaging Mri ◽  
Glucocorticoid Deficiency ◽  
Type 3 ◽  
The Relationship

ContextFamilial glucocorticoid deficiency (FGD) is a rare autosomal recessive ACTH-resistance syndrome characterized by glucocorticoid deficiency in the absence of mineralocorticoid deficiency. Here, we report the case of a young woman with a corticotroph pituitary adenoma as the initial presentation of FGD.Case reportA 15-year-old girl was referred to our institution for a 16 mm pituitary adenoma associated with glucocorticoid deficiency. Clinical and biological features were evocative of FGD. DNA sequencing did not identify mutations in either the melanocortin 2 receptor (MC2R) or the MC2R accessory protein genes, indicating type 3 FGD. Despite adequate glucocorticoid replacement, plasma ACTH levels remained increased and pituitary magnetic resonance imaging (MRI) showed a progression of the tumour size resulting in optic chiasm compression with intra-tumoural haemorrhaging. When the patient was 26 years old, it was decided that she would undergo transsphenoidal surgery. The histomorphological analysis identified a well-individualized pituitary adenoma immunoreactive for ACTH. The proband's sister also exhibited type 3 FGD associated with pituitary hyperplasia upon MRI.ConclusionThis case highlights the relationship between FGD and hyperplasia of ACTH-producing cells, potentially leading to histologically proven pituitary corticotroph adenomas. This observation raises the question of the pituitary MRI's significance in the follow-up of FGD.

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